Tonometry Flashcards
Aqueous Production
Produced by ciliary processes of ciliary body
Mechanism
- Diffusion
- Ultrafiltration
- Active Secretion
Diffusion (Aqueous Production)
- molecules move from high to low conc.
- gradient btn ciliary stroma and capillaries
- counts for SMALL amount of Aqueous Production
Ultrafiltration (Aqueous Production)
- driven by hydrostatic pressure
- fluid moves from area of high pressure to low pressure
- Capillary pressure > IOP
- Aqueous flow towards aqueous stroma
- High IOP = less aqueous produced
- 10%- 20% of aqueous formation
Active Secretion (Aqueous Production)
- accounts for 80%- 90%
- energy dependent
- moves molecules against a conc. gradient
- not IOP dependent
Aqueous Flow
- Formed in ciliary process
- Flows into posterior chamber (PC)
- through lens/iris diaphragm
- Into anterior chamber (AC)
- exits peripheral AC
Aqeuous Convention Current
Aqueous is warmer in posterior AC –> warm aqueous rises –> cools in peripheral AC
Uveoscleral Outflow
(Unconventional)
- 5- 35%
- NOT IOP dependent
Pathway:
1. Uveal TM
2. Ciliary Muscle
3. Suprachoroidal Space
4. Sclera OR anterior ciliary veins & vortex veins
Trabecular Outflow Pathway (Conventional)
- 65 - 95%
- IS IOP dependent
- “increase in IOP –> Increase in Aqueous outflow”
Pathway:
1. Anterior Chamber
2. Uveal TM
3. Corneoscleral TM (filters blood)
4. Juxtacananicular Tissue (micro filter pores)
5. Schelmm’s Canal
6. Aqueous Veins
7. Episcleral venous plexus
8. Superior and Inferior Ophthalmic Veins
9. Cavernous Sinus
10. Jugular Veins
Factors That Affect IOP
IOP
- high IOP –> increase aqueous outflow via TM pathway
Accommodation
- contraction of ciliary muscle –> pulls on TM and opens pores –> increase outflow –> lower IOP
Episcleral Venous Pressure (EVP)
- 1 to 1 relationship in pressure change
- 1 mmHg increase in EVP –> 1mmHg increase IOP
Causes of increase EVP
**Valsalva
- ex: holding breath, straining, coughing
**Gonioscopy
- pressure on the globe
Carotid Cavernous Fistula
Sturge- Weber Syndrome
Long Term Factors affect IOP
*Age - aqueous production decrease, AC angle narrowing
*Trauma - damage, scarring
Race
Sex
Family Hx
Refractive error
Systemic disease (obesity, hypertension)
Medications, Pharmaceutical Agents
Factors causing Transient IOP change
Glaucoma Medications:
*Cholinergic (pilocarpine, Vuity)
- Simulates parasympathetic system
- causes contraction of ciliary muscle, particularly longitudinal fibers insert into TM
- *Causes Accommodation
- pulls TM –> opens pores –> increase outflow via Trabecular pathway –> *Miotic –> Decrease IOP
Pupillary Dilation: Drops
**Anti-Cholinergic
- blocks Acetylcholine receptors on sphincter
- inactivates ciliary muscles –> no accommodation (cycloplegia)
Post Dilated IOP Spike: Possible Mechanisms
Angle Closure (narrow angle) – Takes HOURS to occur
Plateau Iris, Cycloplegic effect of mydriatic agent, pigment release in the AC – occurs SOON after dilation
Angle Closure: (Relative) Pathogenesis Pupillary Block
Mid Dilated Pupil (5-6mm)
- high amnt of apposition from iris to anterior portion of lens (pupil block)
leads to increase in IOP in posterior chamber –> Iris Bombe (anterior bowing of iris) –> angle closure !!
Angles at Risk of Pupillary Block
Angles at Risk
- Grade 1 ( <1/4 : 1 )
- Grade 2 ( =1/4:1)
Widest VH angle will determine if safe to dilate
